Rupture of non-occlusive cerebrovascular lesions, such as intracranial saccular aneurysms or arterio-venous fistulae, is a major cause of stroke. Rupture of an aneurysm causes subarachnoid hemorrhage in which blood from a ruptured vessel spreads over the surface of the brain. About 2.5% of the United States population (4 million Americans) have an unruptured aneurysm. About 100,000 of these people suffer a subarachnoid hemorrhage each year. The disease is devastating, often affecting healthy people in their 40's and 50's, with about half of the rupture victims succumbing within a month, and with half of the survivors becoming seriously disabled as a result of the initial hemorrhage or of a delayed complication.
Neurovascular arteries are generally quite small, having diameters ranging from 2.0 to 4.0 mm in the Circle of Willis, 2.5 to 5.5 mm in the cavernous segment of the internal carotid artery, 1.5 to 3.0 mm in vessels of the distal anterior circulation, and 2.0 to 4.0 mm in the posterior circulation. The incidence of aneurysm varies with the location, with 55% occurring in the Circle of Willis, 30% in the internal carotid, 10% in the distal anterior circulation, and 5% in the posterior circulation.
Screening for these lesions and preventing rupture will lead to better clinical outcomes and lower costs. Non-invasive treatments for ruptured and unruptured lesions are preferred over surgical interventions due to lower costs, lower mortality and morbidity, and patient preference.
One possible treatment for neurovascular aneurysms and other small-vessel abnormalities involves placement of a stent at the site of weakened or damaged vessels. Such a treatment, however, involves several formidable challenges. First, assuming the stent is placed at the target site via a small-diameter catheter, the stent must be flexible enough to allow movement of the catheter along a typically tortuous vascular path, which may involve a number of sharp turns or bends in and through small-diameter vessels, i.e., vessels having diameters in the 2-8 mm range. Second, when the stent is released, it must be capable of expanding from the inner-lumen diameter of the catheter to a diameter somewhat greater than that of the vessel at the target site, requiring an expansion ratio of at least twofold. Third, the stent must provide adequate structural support at the target site to maintain the vessel in a slightly expanded-diameter state. In particular, the stent design should minimize the risk of metal fatigue as the stent is placed between its expanded and compressed forms. Fourth, the stent must provide a low profile and a surface that minimizes the formation of blood thrombi. Finally, the stent should provide an open-network skeleton that allows for delivery of additional agents, e.g., vaso-occlusive coils, through the stent into the underlying aneurysm cavity.
Although a variety of intravascular stents have been proposed heretofore, for example, in U.S. Pat. Nos. 4,512,338, 4,503,569, 4,553,545, 4,795,485, 4,820,298, 5,067,957, 5,551,954, 5,562,641, and 5,824,053, none of these structures adequately meets the several requirements outlined above. In particular, the problem of providing a stent skeletal structure that has a contracted state diameter of 0.5-2 mm, is highly flexible in a contracted state, has a high expansion ratio on delivery from a catheter, and resists metal fatigue on expanding and contracting, has not been adequately solved heretofore.
It would therefore be valuable to provide an intravascular stent, particular one for use in treating neurovascular aneurysms and other vascular abnormalities, that provides the advantages and features mentioned above.